Individuals who have suffered a stroke often demonstrate increased fatigability (exercise induced reductions in force) of the muscles in the paretic leg, which interferes with their ability to walk. In healthy individuals, muscle fatigue is determined by a balance of neural excitation of the muscle and adequate blood flow to the muscle to meet metabolic demands. If the metabolic needs of the muscle are not met, the ability of the muscle to contract is hampered due to both muscle (e.g. build of lactic acid) and neural (decreased neural activation of the muscle) factors. In response to exercise, the cardiovascular system increases blood flow to the exercising muscle by causing vasodilation of the arteries. Normally, increased shear stress of blood flow through arteries during exercise triggers the release of vasodilatory substances (nitric oxide) from the endothelial cells lining the arterial walls. In the chronic stroke population, resting state blood flow is lower in the paretic limb compared with the non-paretic limb due to muscle atrophy. Reduced baseline blood flow limits nitric oxide bioavailability within the vasculature, and can cause endothelial dysfunction. This observation, coupled with deficient neural activation of the paretic muscle during exercise, sets the stage for a dramatically increased rate of neuromuscular fatigue in this subject population. Therefore, our central hypothesis is that endothelial dysfunction in the paretic leg hastens neuromuscular fatigue and worsens task endurance post stroke. To examine this relationship, we will recruit subjects with a diagnosis of unilateral cortical stroke and residual leg paresis. Te following specific aims are proposed: (1) using Doppler ultrasound to quantify stroke-related impairments of femoral artery endothelial function; (2) quantify how modulating blood flow affects measures of neural activation of the muscle during brief contractions and (3) quantify how modulating blood flow affects task duration and neural activation of the muscle during fatiguing contractions. We anticipate that increasing blood flow during fatiguing muscle contractions will significantly increase task duration and neural activation of the test muscle. Th results of this study will be the first to quantify the effects of stroke on conduit artery functio in the leg, and serve as a basis for interventional studies aimed to improve vascular function and blood flow to the paretic musculature in order to optimize force generation and leg function post stroke.